Congenital malformation of nervous systemArini Nurlela03008040

Learning Points Know about the normal embryo developmentKnow about NTDKnow about Spina Bifida

Normal Development

19 Days20 Days23 Days

Neural Tube Defect

Neural Tube Defect Neural tube defects (NTDs) are a group of disorders that arise early in fetal development and can cause life-long complications of varying severity. During the first 3-4 weeks of development, specific cells in an embryo curl up and their edges fuse together to form a narrow tube that becomes the foundation of the spinal cord, brain, and the bone and tissues that surround it. This neural tube fusing process usually is complete by 28 days of gestation before many women even know that they are pregnant. If the tube does not close properly along its entire length, then a NTD will form at the open location. most common birth defects, occurring in approximately one in 1.000 live births in the United States

Causing

Neural Tube Defect (cont)

TreatmentTreatments of NTDs depends on the severity of the complication.

DiscussionSpina Bifida

SPINA BIFIDAOCCULTA

CYSTICAMYELOMENINGOCELEMENINGOCELE

Tatyana McFadden

CONCLUSION

Spinabifidais the most common of a group of birth defects known as neural tube defects, which affect the central nervous system (brain and spinal cord).

Spina bifida begins in the womb, when the tissuesthat foldto form the neural tube do not close or do not stay closed completely. This causes an opening in the vertebrae, which surround and protect the spinal cord. This occurs just a few weeks (21 to 28 days) after conception,usually before the woman knows that she is pregnant.

Spina bifida malformations fall into two catagories,there are spina bifida occulta, spina bifida cystica (meningocele and myelomeningocele). Myelomeningocele is the most significant form and it is this that leads to disability in most affected individuals.

The only known way to prevent spina bifida and other neural tube defects is for the mother to have adequate folic acid levels before and during early pregnancy. This does not work in all cases, but studies have shown that as many as 70% of cases of severe spina bifida could be prevented by adequate folic acid intake.

References1.Markum A.H. Buku Ajar Ilmu Kesehatan Anak, Jakarta : EGC, 2002.

2. Kent, George C.; Robert K. Carr. Comparative Anatomy of the Vertebrates: Ninth Edition. New York, NY, USA: McGraw-Hill Higher Education. pp.408.2001

3. Sadler,T.W.Embriologi Kedokteran Langman.Edisi 10.Jakarta : EGC,2009.

4. Menkes,John H; Till,Kenneth.Text Book of Child Neurology. Philadelphia : Lippincott Williams and Wilkins,1995

5. Holmes,Lewis B. Journal of Pediatrics Vol. 120, Issue 6, Pages 918-919.1992

6. http://www.nlm.nih.gov/medlineplus/spinabifida.html.Accessed June 15 ,2011

Days of gestationEventEffect of toxic stimulus0-18Three germ layers elaborate and early neural plate formsNo effect /death18Neural plate and groove developmentAnterior midline defects22-23Optic vesicles appearinduction hydrocephalus24-26Anterior neuropore closedAnencephaly26-28Posterior neuropore closed,ventral horns formCranium bifidum,spina bifida cystica,spina bifida occulta28-32Anterior and posterior nerve roots form32Cerebellar primordium,vascular circulationMicrocephaly,proliferation syndrome,migration anomalies33-35Prosencephalon claves to form paired telencephalon. Five cerebral vesicles, choroid plexi, dorsal root ganglion developHoloprosencephaly 41Region of olfactory bulb appears in fore brainArhinencephaly 56Differentiation of cerebral cortex, meninges, ventricular foramina, CSF circulationDandy-walker syndrome70-100Corpus callosumAgenesis of corpus calllosum70-150Primary fissures of cerebral cortex ,spinal cord ends at L3 levelLissencephaly, pachygyria140-175Neuronal proliferation in cerebral cortex endsDefects of cellular architectonic , myelin defects7-9 monthsSecondary and tertiary sulciDestructive pathologic changes first noted175 days-4 years postnatallyNeuronal migration, glial cell production. Myelin formation, axosomatic and axodendritic synaptic connections, spinal cord ends L1-L2 level